Rat Sertoli cells express an inducible nitric oxide synthase isoform (iNOS) in response to the combined addition of the cytokines--interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF alpha), interleukin-1alpha (IL-1alpha)--and lipopolysaccharides (LPS). We demonstrated that the addition of cytokines and lipopolysaccharides (C+L) to cultured peritubular cells resulted in high nitrite and iNOS mRNA levels, indicating the induction of an iNOS isoform. This enzyme was not induced in cultured pachytene spermatocytes or spermatids. Nitrite production in Sertoli cells and peritubular cells required both IFNgamma and TNF alpha and was potentiated by LPS, whereas IL-1alpha was ineffective. The induction of nitrite production and iNOS mRNA by IFNgamma+TNF alpha+LPS could be further enhanced by basic fibroblast growth factor in Sertoli cells but not in peritubular cells. In contrast, transforming growth factor beta markedly reduced this induction in peritubular cells but had no effect on Sertoli cells. FSH positively modulated the C+L-induced iNOS in Sertoli cells. Dibutyryl cAMP had a synergistic effect with C+L on NOS activity in both Sertoli cells and peritubular cells. In contrast, testosterone did not influence basal or induced NOS activity in these two cell types. These data show that NOS activity in the somatic cells of the seminiferous tubules is induced and regulated by multiple factors that act in combination, and suggest that nitric oxide may participate in the endocrine and paracrine control of testicular function.
Mice with a targeted disruption of the prolactin (PRL) receptor gene were used to study the physiological role of PRL in the control of the male reproductive function. Fertility parameters as well as body and reproductive organ weights (epididymis and testes) were unaffected in PRL receptor knockout mice. Testicular histology and sperm reserves were also normal. Compared with wild-type animals, knockout mice had no significant difference in basal plasma LH, FSH, and testosterone levels, and the weight of seminal vesicles and prostate was unaffected. Moreover, no alteration was detected in human chorionic gonadotropin-induced testosterone levels. It is concluded that the absence of PRL signaling is not detrimental to male testicular function and to fertility in the mouse.
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